Dataset Information

Six Weeks of Morning Fasting Causes Little Adaptation of Metabolic or Appetite Responses to Feeding in Adults with Obesity.

ABSTRACT:

Objective

The aim of this study was to determine the effects of sustained morning fasting or breakfast consumption on metabolism, energy intake, and appetite in healthy adults with obesity.

Methods

An independent-measures randomized controlled trial with baseline and follow-up laboratory assessment days separated by a 6-week intervention of either morning fasting (0 kcal until 12:00 pm) or daily breakfast (> 700 kcal by 11:00 am) was performed. Measures included metabolic outcomes (glucose, insulin, nonesterified fatty acids), hormones regulating appetite (total/acylated ghrelin, peptide YY, leptin), and energy expenditure (diet-induced thermogenesis) parameters throughout a laboratory test day and ad libitum intake following a fixed breakfast.

Results

Allocation to fasting versus breakfast resulted in minimal adaptation as reflected by the metabolic outcomes or the majority of appetite regulatory outcomes for either area under curve or time-course-based measures (P > 0.05). Ad libitum lunch intake was not different (P = 0.13), nor was diet-induced thermogenesis or a composite appetite score (both P > 0.10). However, there was a reduced total area under the curve for peptide YY (P = 0.05) and increased postprandial hunger ratings (P = 0.05) in the breakfast group.

Conclusions

There was little evidence of metabolic adaptation to acute feeding or negative consequences from sustained morning fasting. This indicates that previously observed differences between breakfast consumers and skippers may be acute effects of feeding or may have resulted from other lifestyle factors.

SUBMITTER: Chowdhury EA

PROVIDER: S-EPMC6519370 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Six Weeks of Morning Fasting Causes Little Adaptation of Metabolic or Appetite Responses to Feeding in Adults with Obesity.

Chowdhury Enhad A EA Richardson Judith D JD Gonzalez Javier T JT Tsintzas Kostas K Thompson Dylan D Betts James A JA

Obesity (Silver Spring, Md.) 20190329 5

<h4>Objective</h4>The aim of this study was to determine the effects of sustained morning fasting or breakfast consumption on metabolism, energy intake, and appetite in healthy adults with obesity.<h4>Methods</h4>An independent-measures randomized controlled trial with baseline and follow-up laboratory assessment days separated by a 6-week intervention of either morning fasting (0 kcal until 12:00 pm) or daily breakfast (> 700 kcal by 11:00 am) was performed. Measures included metabolic outcomes ...[more]

PMID: 30925197

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Project description:RDH1 is one of the several enzymes that catalyze the first of the two reactions to convert retinol into all-trans-retinoic acid (atRA). Here, we show that Rdh1-null mice fed a low-fat diet gain more weight as adiposity (17% males, 13% females) than wild-type mice by 20 weeks old, despite neither consuming more calories nor decreasing activity. Glucose intolerance and insulin resistance develop following increased adiposity. Despite the increase in white fat pads, epididymal white adipose does not express Rdh1, nor does muscle. Brown adipose tissue (BAT) and liver express Rdh1 at relatively high levels compared to other tissues. Rdh1 ablation lowered body temperatures during ambient conditions. Given the decreased body temperature, we focused on BAT. A lack of differences in BAT adipogenic gene expression between Rdh1-null mice and wild-type mice, including Pparg, Prdm16, Zfp516 and Zfp521, indicated that the phenotype was not driven by brown adipose hyperplasia. Rather, Rdh1 ablation eliminated the increase in BAT atRA that occurs after re-feeding. This disruption of atRA homeostasis increased fatty acid uptake, but attenuated lipolysis in primary brown adipocytes, resulting in increased lipid content and larger lipid droplets. Rdh1 ablation also decreased mitochondrial proteins, including CYCS and UCP1, the mitochondria oxygen consumption rate, and disrupted the mitochondria membrane potential, further reflecting impaired BAT function, resulting in both BAT and white adipose hypertrophy. RNAseq revealed dysregulation of 424 BAT genes in null mice, which segregated predominantly into differences after fasting vs after re-feeding. Exceptions were Rbp4 and Gbp2b, which increased during both dietary conditions. Rbp4 encodes the serum retinol-binding protein-an insulin desensitizer. Gbp2b encodes a GTPase. Because Gbp2b increased several hundred-fold, we overexpressed it in brown adipocytes. This caused a shift to larger lipid droplets, suggesting that GBP2b affects signaling downstream of the ?-adrenergic receptor during basal thermogenesis. Thus, Rdh1-generated atRA in BAT regulates multiple genes that promote BAT adaptation to whole-body energy status, such as fasting and re-feeding. These gene expression changes promote optimum mitochondria function and thermogenesis, limiting adiposity. Attenuation of adiposity and insulin resistance suggests that RDH1 mitigates metabolic syndrome.

Project description:BackgroundFood parenting practices are associated with child weight. Such associations may reflect the effects of parents' practices on children's food intake and weight. However, longitudinal, qualitative, and behavioral genetic evidence suggests these associations could, in some cases, reflect parents' response to children's genetic risk for obesity, an instance of gene-environment correlation. We tested for gene-environment correlations across multiple domains of food parenting practices and explored the role of parent-reported child appetite in these relationships.Materials and methodsData on relevant variables were available for N = 197 parent-child dyads (7.54 ± 2.67 years; 44.4% girls) participating in RESONANCE, an ongoing pediatric cohort study. Children's body mass index (BMI) polygenic risk score (PRS) were derived based on adult GWAS data. Parents reported on their feeding practices (Comprehensive Feeding Practices Questionnaire) and their child's eating behavior (Child Eating Behavior Questionnaire). Moderation effects of child eating behaviors on associations between child BMI PRS and parental feeding practices were examined, adjusting for relevant covariates.ResultsOf the 12 parental feeding practices, 2 were associated with child BMI PRS, namely, restriction for weight control (β = 0.182, p = 0.011) and teaching about nutrition (β = -0.217, p = 0.003). Moderation analyses demonstrated that when children had high genetic obesity risk and showed moderate/high (vs. low) food responsiveness, parents were more likely to restrict food intake to control weight.ConclusionOur results indicate that parents may adjust their feeding practices in response to a child's genetic propensity toward higher or lower bodyweight, and the adoption of food restriction to control weight may depend on parental perceptions of the child's appetite. Research using prospective data on child weight and appetite and food parenting from infancy is needed to further investigate how gene-environment relationships evolve through development.

Dataset Information

Six Weeks of Morning Fasting Causes Little Adaptation of Metabolic or Appetite Responses to Feeding in Adults with Obesity.

Objective

Methods

Results

Conclusions

Publications

Six Weeks of Morning Fasting Causes Little Adaptation of Metabolic or Appetite Responses to Feeding in Adults with Obesity.

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